It has been generally accepted that the primary event in gene expression is asymmetric, in the sense that only one of the two DNA strands in the gene serves as a template for RNA. However, during the last two years, I have shown that at least in the mitochondrial genetic system in HeLa cells and in the DNA tumor virus SV40 late during infection, the concept of asymmetric transcription is wrong and the alternative possibility, that of symmetrical transcription, is taking place. Symmetrical transcription predicts regulation of gene expression at the post-transcriptional level and it involves the selective degradation of particular RNA sequences. Using model systems that involve mainly the various interactions between polyoma and SV40 DNA tumor viruses and the cell, I propose to determine whether these viruses are transcribed symmetrically early in infection and in transformed cells and whether cellular DNA sequences that are covalently linked to the viral DNA are also transcribed in a symmetrical fashion as a consequence of the integration of the viral genome. In addition, transcription from circular viral DNA will be compared with the mode of transcription of genes from linear DNA tumor viruses (Adeno and Herpes) and to genes from normal cells. If post-transcriptional regulation of gene expression proves to be a widespread phenomenon, the aspects of how selective RNA degradation is achieved will be studied. Finally, the biological implications of symmetrical transcription in relation to the occurrence of double-stranded RNA in normal and cancer cells will be investigated.